Brain Trauma Stroke
Figure 1: Course of the Pyramidal Tract and Alternate Motor Fibres from the Motor Cortex to the Pons
Precentral gyrus
of the microstructural status of designated regions of interest or reconstructed tracts.20
and human FA is calculated from directional diffusivities
Internal capsule
Axial diffusivity is thought to be an indicator of axonal integrity, whereas radial diffusivity was suggested to primarily reflect (de-)myelination. However, the model of a specific relationship of directional diffusivities with discrete pathological processes is controversial, especially in regions of complex fibre architecture.26 Using diffusivity parameters, fibre degeneration has been revealed in previous studies.27–30
and the quantification of damage to descending motor
(axial and radial), which by themselves have been found to reflect the microstructural status of white matter in animal21,22 studies.23–25
Furthermore, the DTI-based reconstruction of
tracts allowed for an evaluation of the topographic relation of a lesion to corticospinal fibres,31–36 and tracts14 tracts.1,17,37
the calculation of the overlap between lesion
Anterior pons
Posterior pons
The correlations of established motor impairment scores with those DTI-derived measures revealed that DTI can in fact be used as a structural surrogate marker of the amount of damage to corticospinal tracts and, thus, their functional integrity.5
Transcallosal Motor Fibres
Pyramidal tract (PT) and alternate motor fibres (aMF) take a similar course as they descend to the level of the internal capsule and begin to separate before entering the cerebral peduncles. The aMF takes a more dorsal route in the mid-brain and brainstem so that both fibre bundles can be clearly distinguished in the pons, with the PT being located at the base of the pons and the aMF in the tegmentum pontis. Source: Lindenberg et al., 2010.17
In contrast, larger infarcts usually affect multiple brain systems, which may result in complex neurological syndromes including hemispatial neglect or apraxia. However, involvement of the white matter has not received much attention until recently but was found to be particularly prominent in large cerebral infarcts with and without hemispatial neglect, apraxia and severe hemiparesis.8–11 Notably, it is important to remember that it is not simply the size of the infarct, but preferentially its location that determines the outcome after stroke.12–14
that can be localised to this very same area when probed in healthy subjects.6,7
Corticospinal Motor Fibres
The importance of corticospinal fibres for recovery of motor function after stroke has been demonstrated with imaging and electrophysiological measures.12
Interestingly, clinical and
we hypothesise that aMF comprise polysynaptic cortico-reticulo- and cortico-rubro-spinal tracts. The functional integrity of corticospinal motor fibres can be investigated using electrophysiological measures. Transcranial magnetic stimulation (TMS) has been shown to strongly correlate with motor impairment in the acute and subacute phase, whereas its predictive value varied between studies in the chronic stage after stroke.19
In one study, a
combination of TMS with DTI-derived parameters proved to be useful in estimating a patient’s potential for recovery when undergoing an intensive motor rehabilitation programme even years after the stroke.1 The most commonly used DTI parameter is fractional anisotropy (FA), which indicates the coherence of aligned fibres and allows inferences
68
despite visible damage to the PT. Using DTI imaging as a way of visualising fibre tracts, these alternate motor fibres have recently been visualised (see Figure 1) and their role for motor recovery after stroke has been demonstrated.17 animal work,18
electrophysiological techniques suggested the presence of alternate descending motor fibres (aMF) in addition to the pyramidal tract (PT) since motor evoked potentials (MEP) could still be elicited from the ipsilesional motor cortex15 possible16
On the basis of evidence from
In the future, more accurate estimations of recovery potential might be possible when considering not only corticospinal tracts (PT and aMF), but also transcallosal motor fibres. Models of an imbalance in inter-hemispheric interactions after stroke highlight the important role of transcallosal connections for recovery.38
Similarly, functional
imaging studies demonstrated an alteration of inter-hemispheric connectivity patterns after stroke,39,40
and experimental non-invasive
brain stimulation studies revealed that facilitation of motor recovery can be achieved via upregulation of intact ipsilesional motor cortex and via downregulation of contralesional motor cortex.41
Thus, there
Work in healthy subjects, in which the association of function and microstructure of transcallosal motor connection was demonstrated,44
is ample evidence for the importance of inter-hemispheric interactions in motor recovery after stroke, although the exact role of contralesional primary and non-primary motor regions remains elusive.42,43
led to an investigation of those tracts in chronic stroke patients undergoing non-invasive brain stimulation. It could be shown that DTI-derived measures of transcallosal motor-to-motor fibres allowed predictions of therapeutic response to experimental rehabilitation: the more the diffusivity profiles resembled those observed in healthy subjects, the greater a patient’s potential for functional recovery.45
and selective finger movement was The Role of Perilesional Tissue
As the area of ischaemia typically exceeds the resulting infarct lesion,46–49
an important factor contributing to recovery is the perilesional tissue. The perilesional tissue is supposed to be structurally intact but functionally altered due to transient ischaemia and subsequent reperfusion. Both factors evoke a large number of biochemical, metabolic and immunological processes that evolve sequentially.50
Notably, the binding of flumazenil, a γ-aminobutyric acid
(GABA)A receptor antagonist, as measured with positron emission tomography, was found to be reduced in this area in proportion
to the initial hypoperfusion as assessed with perfusion computed tomography.51
This suggests loss of inhibitory interneurons in the peri-infarct area and consecutive increased cortical excitability, as demonstrated in TMS studies.52,53
The functionally abnormal
perilesional tissue contributes to the clinical deficit, which will affect an activation-related signal: functional MRI (fMRI) performed approximately two days after stroke revealed an area in the
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